- Email: [email protected]
Hypertension after coronary operation
J
THORAC CARDIOVASC SURG
81:396-399, 1981
Hypertension after coronary operation Can it be prevented by pulsatile perfusion? Nonpulsatile perfusion during cardiopulmonary bypass (CPB) has been implicated as a causative factor of postoperative hypertension. In a consecutive series, patients undergoing coronary bypass were selected for perfusion with either nonpulsatile flow (American Optical roller pump) or pulsatile flow (Desjardin's modification of the roller pump). The incidence of postoperative hypertension and the levels of peripheral renin were noted. No differences could be observed in renin activity, with either modality of perfusion, before CPB, after 30 minutes of stable CPB, or 2 hours postoperatively. Hypertension, necessitating treatment, occurred in 60% of the patients having pulsatile and 68% of those having nonpulsatile perfusion (p > 0.05). Although pulsatile CPB would appear to be more physiological than nonpulsatile perfusion, this method of creating pulsatile flow does not appear to eliminate postoperative hypertension.
Tomas A. Salerno, M.D., Michael Henderson, M.Sc., M.D.,* Fraser M. Keith, M.D., and Edward J. P. Charrette, M.D., Kingston, Ontario, Canada
Postoperative hypotension and the low-output syndrome are now rarely encountered during cardiac operations because of better understanding and better measures taken intraoperatively to protect the myocardium. A new entity, postoperative hypertension, has since evolved. Although its cause remains unknown, the nonphysiological characteristics of nonpulsatile perfusion during cardiopulmonary bypass (CPB) appear to be an important factor. The present study is a clinical evaluation of a new pulsatile device in terms of (1) the incidence of postoperative hypertension and (2) renin activity during and after CPB.
Materials and patients Fifty-nine consecutive patients undergoing elective coronary artery bypass operation were subjected to either pulsatile (37 patients) or nonpulsatile (22 patients) perfusion. Rather than alternate the perfusion From the Departments of Surgery and Medicine, Queen's University, Kingston, Ontario, Canada. Supported by the Ontario Heart Foundation, Grant 2-4. Received for publication Dec. 4, 1979. Accepted for publication July 8, 1980. Address for reprints: Dr. T. Salerno, Department of Surgery, Queen's University, Kingston, Ontario, Canada. *Department of Medicine.
396
system from one patient to the next, we subjected blocks of patients to pulsatile or nonpulsatile flow in the following sequence: 27 pulsatile, 15 nonpulsatile, 10 pulsatile, and seven nonpulsatile. For the 37 patients receiving pulsatile perfusion, the pulsatile device was an adaptation of the extra pump head in the American Optical roller pump, as recently described by Desjardin and associates. I The number of strokes per minute varied between 60 and 70. A representative pressure tracing taken during an operation is shown in Fig. I. Analysis of all pressure tracings revealed the steepness of the pulse ascent to be 123.3 ± 7 mm/sec. The heights of the peaks and the depths of the troughs were 101 ± 8 mm Hg and 61 ± 9 mm Hg, respectively. None of the patients had a history of hypertension preoperatively. All received propranolol prior to operation, including on the morning of the operation. The patients received the same premedications (meperidine or diazepam and atropine). They were then given oxygen, and anesthesia was induced with thiopental sodium and succinylcholine. Anesthesia was maintained with intravenous morphine and nitrous oxide-oxygen or halothaneoxygen mixtures. Normothermic CPB was instituted with the American Optical roller pump using an 8.5 Morris aortic cannula. Mean pump time was 93 minutes for the pulsatile perfusion group and 86 minutes for the nonpulsatile group. A mean of 3.1 grafts per patient were received by each group. Cardioplegic ar-
0022-5223/81/030396+04$00.40/0 © 1981 The C. V. Mosby Co.
Volume 81
Hypertension after coronary operation
Number 3
3 97
March,1981
l
Pulsatile Pump on Fig. 1. Nonpulsatile and pulsatile pressure tracing during cardiopulmonary bypass. BP, Blood pressure. rest* was routinely used. The heart was kept at 15° to 20° C with repeated infusions of cardioplegic solution at 20 minute intervals and by topical cooling. The temperature of the systemic perfusate and the body temperature were kept at normal levels. Peripheral levels of renint were determined prior to the institution of CPB, after 30 minutes of stable perfusion, and 2 hours postoperatively. Blood gases and hematocrit values were similar in the two groups. Urinary output was monitored intraoperatively, and the systemic peripheral resistance (SPR) was calculated. Postoperative hyper" tension was defined as a systolic blood pressure equal to or greater than 160 mm Hg and/or diastolic pressure greater than 90 mm Hg, despite adequate anesthesia intraoperatively and sedation and/or analgesics postoperatively. Treatment consisted of nitroprusside infusion to maintain the blood pressure at preoperative values. Postoperative hypoxia, shivering, and hypothermia were ruled out as possible factors contributing to the hypertensive state. Mean age for the group receiving pulsatile perfusion was 55 years and that for the group having nonpulsatile perfusion, 49 years. Results
There were no deaths in the series, and no complications could be attributed to the pulsatile device. Intraoperative pump flows averaged 5.3 ± 0.7* Llmin during pulsatile and 5.0 ± 0.5 Llmin during nonpulsatile perfusion. Mean perfusion pressure was 86 ± 6.2 *Cardioplegic solution: 500 mllactated Ringer's, 10 mEq KCI, 12.5 mEq sodium bicarbonate, 12 ml 2% lidocaine, 17 ml 50% dextrose, 124 mg Solu-Cortef, pH 7.7, temperature 4° C. tRadioimmunoassay, New England Nuclear Biomedical Assay Laboratory, Boston, Mass. :j:Standarddeviation of the mean.
and 88 ± 5.6 mm Hg, respectively. Intraoperative urinary output averaged 5.0 ± 1.5 mIl min in the pulsatile perfusion and 5.3 ± 2 ml/min in the nonpulsatile perfusion groups. Postoperatively, it was difficult to accurately assess and compare urine output, as some patients had received diuretics and their fluid balances differed. All patients with postoperative hypertension, as defined in the Materials and patients section, became hypertensive from 0 to 6 hours postoperatively and were treated accordingly. Hypertension was present in 22 of 37 patients (60%) receiving pulsatile perfusion. In the subsequent 6 to 24 hours, 12 of these 22 patients (55%) required continued antihypertensive treatment. Among the patients subjected to nonpulsatile perfusion, 15 of 22 (68%) were hypertensive at 0 to 6 hours; from 6 to 24 hours, seven of these 15 patients (47%) still required nitroprusside. There was no significant difference (p > 0.05)* in the number of hypertensive patients between the two groups. Pre-CPB renin determinations averaged 2.8 ± 1.3 ng/mIlhr in the patients having pulsatile perfusion and 2.3 ± 0.4 ng/mIlhr in those having nonpulsatile perfusion (p > 0.05); after 30 minutes of normothermic perfusion, mean renin levels remained at 2.7 ± 1.2 and 2.7 ± 1.9 ng/mIlhr, respectively (p > 0.05). The hypertensive patients subjected to pulsatile perfusion had renin levels of 3.7 ± 1.9 ng/mIlhr, compared with 3.2 ± 0.7 ng/mIlhr for those having nonpulsatile perfusion (p > 0.05). The normotensive patients had renin levels of 2.6 ± 0.8 and 2.4 ± 0.5 ng/mIlhr, respectively. The difference in renin levels between hypertensive and normotensive patients was significant (p < 0.05), whereas the difference in renin between *Analysis of variance.
The Journal of
398
Salerno et al.
hypertensive patients in the pulsatile and nonpulsatile perfusion groups was not (p > 0.05). Intraoperative SPR was calculated at 1,600 ± 130 dynes/sec/em:" for the pulsatile and 1,760 ± 80 dynes/sec/em." for the nonpulsatile perfusion group (p > 0.05). Postoperative SPR was not calculated, because cardiac output is not routinely determined in our practice. Discussion Postoperative hypertension occurs in 33% to 58% of patients undergoing cardiac operations, 2-4 and the cause remains unknown. Nonpulsatile perfusion during CPB has been implicated as an etiologic factor, 4-6 and pulsatile flow appears to decrease the incidence of postoperative hypertension. S The systemic peripheral resistance (SPR) has been shown to be elevated during pulseless perfusion.v 4 whereas with pulsatile flow the SPR is significantly lower. 7. 8 The renin-angiotensin system and catecholamines'': 9 are contributing factors in this condition. A rise in peripheral renin levels has been demonstrated with nonpulsatile perfusion, possibly the result of either (1) direct stimulation of the juxtaglomerular apparatus by the absence of the pulse pressure" or (2) the redistribution of cortical blood flow due to vasoconstriction of the outer renal cortex. 10 Loss of pulse pressure during nonpulsatile CPB may also stimulate the carotid baroreceptors, so that the kidneys secrete more renin. 11 Pulsatile perfusion is also known to prevent the depressive effects on the pituitary gland observed during nonpulsatile flow. 12 In addition to the possible benefit of preventing postoperative hypertension, pulsatile perfusion appears to be more physiological than nonpulsatile flow. 6. 13. 14 Even so, surgeons have been reluctant to use it because of the unreliability of the systems available, the complexity of the apparatus, and the pressure gradients across the arterial cannula. Our study employed the technique of pulsatile perfusion described by Desjardin and associates. 1 This system delivers pulsatile perfusion which has a pressure tracing similar to normal cardiac action (Fig. 1). We 1S have demonstrated that the degree of hemolysis is comparable to that of nonpulsatile perfusion. Our results show that adding pulsatile perfusion to our standard American Optical roller pump did not affect the incidence of postoperative hypertension, as it occurred in 60% of the patients subjected to pulsatile perfusion and 68% of those subjected to nonpulsatile perfusion. In addition, renin levels were similar in the two groups during CPB and 2 hours after operation. It is interesting to note that both groups of patients had high renin levels even prior to CPB. The
Thoracic and Cardiovascular Surgery
reason for this observation, also noted by Frater, 16 remains unknown. It may be that factors such as diet, innate anxiety, and presurgical anxiety affect renin release in these patients. The hypertensive patients had higher renin levels postoperatively than the normotensive patients. However, there was a high variability in renin levels, as shown on the standard deviations of the mean. Thus nonpulsatile flow may not be the only underlying etiologic factor responsible for the hypertensive episode. For example, the mechanism may be a generalized disturbance related to the sympathetic overdrive, rather than resulting from improved cardiac performance after operation. 17 It has also been postulated that abnormal vasomotor responses may be involved, via an unstable feedback mechanism of the cardiac and/or aortic pressor receptors. 18-22 The role of catecholamines and other vasoactive agents, such as serotonin;" has been demonstrated previously in this condition. Since completion of this study we have routinely used pulsatile perfusion during CPB because of its theoretical advantages. However, we have been unable to decrease the incidence of hypertension after cardiac procedures. Much research remains to be done in this continuing effort to elucidate the mechanism underlying postoperative hypertension. REFERENCES Desjardin J, Maille JG, LussierCP, Grondin P: A simple device for achieving pulsatile flow during cardiopulmonary bypass. Ann Thorac Surg 27:178-180, 1979 2 Estefanous FG, Tarazi RC, Viljoen JF, EI Tawil MY: Systemic hypertension following myocardial revascularization. Am Heart J 85:732-738, 1973 3 Hoar PF, Hickey RF, Ullyot OJ: Systemic hypertension following myocardial revascularization. A method of treatment using epidural anesthesia. J THORAC CARDIOVASC SURG 71:859-864, 1976 4 Roberts AJ, Niarchos AP, Subramanian VA, Abel RM, Herman SO, Sealey JE, Case DB, White RP, Johnson GA, Laragh JH, Gay WA: Systemic hypertension associated with coronary artery bypass surgery. Predisposing factors, hemodynamic characteristics, humoral profile, and treatment. J THORAC CARDIOVASC SURG 74:846-859, 1977 5 Landyrnore RW, Murphy DA, Kinley CE, Parrott JG, Moffitt EA, Longley WJ, Qirbi AA: Does pulsatile flow influence the incidence of postoperative hypertension? Ann Thorac Surg 28:261-268, 1979 6 Many M, Giron G, Birtwell WC, Deterling RA Jr, Soroff HS: Effectsof depulsation of renal blood flow upon renal function and renin secretion. Surgery 66:242-249, 1969 7 Jacobs LA, Klopp EH, Seamone W, Topaz SR, Gott VL: Improved organ function during cardiac bypass with a
Volume 81
Hypertension after coronary operation
Number 3
3 99
March,1981
roller pump modified to deliver pulsatile flow. J THORAC CARDIOVASC SURG 58:703-712, 1969 8 Trinkle JK, Helton NE, Bryant LR, Griffen WO: Pulsatile cardiopulmonary bypass. Clinical evaluation. Surgery
16 17
68:1074-1078, 1970 9 Laragh JH, Baer L, Brunner HR, Buhler FR, Sealey JE, Vaughan DE: Renin, angiotensin and aldosterone system in pathogenesis and management of hypertensive vascular disease. Am J Mcd 52:633-652, 1972 10 Goodman TA, Gerard DF, Bernstein EF, Dilley RB: The effects of pulseless perfusion on the distribution of renal cortical blood flow and on renin release. Surgery 80:31-
39, 1976 II Edmunds LH: Discussion of Landymore et aP 12 Taylor KM, Wright GS, Bain WH, Caves PK, Beastall GS: Comparative studies of pulsatile and nonpulsatile flow during cardiopulmonary bypass. III. Response of anterior pituitary gland to thyrotropin-releasing hormone. J THORAC CARDIOVASC SURG 75:579-584, 1978 13 Dunn J, Kirsh MM, Harness J, Carroll M, Straker J, Sloan H: Hemodynamic, metabolic, and hemotologic effects of pulsatile cardiopulmonary bypass. J THORAC CARDIOVASC SURG 68:138-147, 1974 14 Salerno TA, Shizgal HM, Dobell ARC: Pulsatile perfusion. Its effects on blood flow distribution in hypertrophied hearts. Ann Thorac Surg 27:559-563, 1979 15 Salerno TA, Charrette EJP, Keith FM: Hemolysis during
18
19 20
pulsatile perfusion. Clinical evaluation of a new device. J THORAC CARDIOVASC SURG 79:579-581, 1980 Frater RWM: Discussion of Landymore et al 5 Fouad FM, Estefanous FG, Tarazi RC: Hemodynamics of postmyocardial revascularization hypertension. Am J Cardiol 41:564-569, 1978 Estefanous FG, Tarazi RC, Buckley S, Taylor PC: Arterial hypertension in immediate postoperative period after valve replacement. Br Heart J 40:718-724, 1978 Viljoen JF, Estefanous FG, Tarazi RC: Acute hypertension immediately after coronary artery surgery. J THORAC CARDIOVASC SURG 71:548-550, 1976 Hanson EL, Kane PB, Askanazi J, Neville JF, Webb WR: Comparison of patients with coronary artery or valve disease. Intraoperative differences in blood volume and observations of vasomotor response. Ann Thorac Surg
22:343-346, 1976 21 Liard JF, Tarazi RC, Ferrario CM, Manger WM: Hemodynamic and humoral characteristics of hypertension induced by prolonged stellate ganglion stimulation in conscious dogs. Circ Res 36:455-464, 1975 22 Peterson DF, Brown AM: Pressor reflexes produced by stimulation of afferent fibers in cardiac sympathetic nerves of the cat. Circ Res 28:605-610, 1971 23 Replogle R, Levy M, DeWall RA, Lillehei RC: Catecholamine and serotonin response to cardiopulmonary bypass. J THORAC CARDIOVASC SURG 44:638-648, 1962
THORAC CARDIOVASC SURG
81:396-399, 1981
Hypertension after coronary operation Can it be prevented by pulsatile perfusion? Nonpulsatile perfusion during cardiopulmonary bypass (CPB) has been implicated as a causative factor of postoperative hypertension. In a consecutive series, patients undergoing coronary bypass were selected for perfusion with either nonpulsatile flow (American Optical roller pump) or pulsatile flow (Desjardin's modification of the roller pump). The incidence of postoperative hypertension and the levels of peripheral renin were noted. No differences could be observed in renin activity, with either modality of perfusion, before CPB, after 30 minutes of stable CPB, or 2 hours postoperatively. Hypertension, necessitating treatment, occurred in 60% of the patients having pulsatile and 68% of those having nonpulsatile perfusion (p > 0.05). Although pulsatile CPB would appear to be more physiological than nonpulsatile perfusion, this method of creating pulsatile flow does not appear to eliminate postoperative hypertension.
Tomas A. Salerno, M.D., Michael Henderson, M.Sc., M.D.,* Fraser M. Keith, M.D., and Edward J. P. Charrette, M.D., Kingston, Ontario, Canada
Postoperative hypotension and the low-output syndrome are now rarely encountered during cardiac operations because of better understanding and better measures taken intraoperatively to protect the myocardium. A new entity, postoperative hypertension, has since evolved. Although its cause remains unknown, the nonphysiological characteristics of nonpulsatile perfusion during cardiopulmonary bypass (CPB) appear to be an important factor. The present study is a clinical evaluation of a new pulsatile device in terms of (1) the incidence of postoperative hypertension and (2) renin activity during and after CPB.
Materials and patients Fifty-nine consecutive patients undergoing elective coronary artery bypass operation were subjected to either pulsatile (37 patients) or nonpulsatile (22 patients) perfusion. Rather than alternate the perfusion From the Departments of Surgery and Medicine, Queen's University, Kingston, Ontario, Canada. Supported by the Ontario Heart Foundation, Grant 2-4. Received for publication Dec. 4, 1979. Accepted for publication July 8, 1980. Address for reprints: Dr. T. Salerno, Department of Surgery, Queen's University, Kingston, Ontario, Canada. *Department of Medicine.
396
system from one patient to the next, we subjected blocks of patients to pulsatile or nonpulsatile flow in the following sequence: 27 pulsatile, 15 nonpulsatile, 10 pulsatile, and seven nonpulsatile. For the 37 patients receiving pulsatile perfusion, the pulsatile device was an adaptation of the extra pump head in the American Optical roller pump, as recently described by Desjardin and associates. I The number of strokes per minute varied between 60 and 70. A representative pressure tracing taken during an operation is shown in Fig. I. Analysis of all pressure tracings revealed the steepness of the pulse ascent to be 123.3 ± 7 mm/sec. The heights of the peaks and the depths of the troughs were 101 ± 8 mm Hg and 61 ± 9 mm Hg, respectively. None of the patients had a history of hypertension preoperatively. All received propranolol prior to operation, including on the morning of the operation. The patients received the same premedications (meperidine or diazepam and atropine). They were then given oxygen, and anesthesia was induced with thiopental sodium and succinylcholine. Anesthesia was maintained with intravenous morphine and nitrous oxide-oxygen or halothaneoxygen mixtures. Normothermic CPB was instituted with the American Optical roller pump using an 8.5 Morris aortic cannula. Mean pump time was 93 minutes for the pulsatile perfusion group and 86 minutes for the nonpulsatile group. A mean of 3.1 grafts per patient were received by each group. Cardioplegic ar-
0022-5223/81/030396+04$00.40/0 © 1981 The C. V. Mosby Co.
Volume 81
Hypertension after coronary operation
Number 3
3 97
March,1981
l
Pulsatile Pump on Fig. 1. Nonpulsatile and pulsatile pressure tracing during cardiopulmonary bypass. BP, Blood pressure. rest* was routinely used. The heart was kept at 15° to 20° C with repeated infusions of cardioplegic solution at 20 minute intervals and by topical cooling. The temperature of the systemic perfusate and the body temperature were kept at normal levels. Peripheral levels of renint were determined prior to the institution of CPB, after 30 minutes of stable perfusion, and 2 hours postoperatively. Blood gases and hematocrit values were similar in the two groups. Urinary output was monitored intraoperatively, and the systemic peripheral resistance (SPR) was calculated. Postoperative hyper" tension was defined as a systolic blood pressure equal to or greater than 160 mm Hg and/or diastolic pressure greater than 90 mm Hg, despite adequate anesthesia intraoperatively and sedation and/or analgesics postoperatively. Treatment consisted of nitroprusside infusion to maintain the blood pressure at preoperative values. Postoperative hypoxia, shivering, and hypothermia were ruled out as possible factors contributing to the hypertensive state. Mean age for the group receiving pulsatile perfusion was 55 years and that for the group having nonpulsatile perfusion, 49 years. Results
There were no deaths in the series, and no complications could be attributed to the pulsatile device. Intraoperative pump flows averaged 5.3 ± 0.7* Llmin during pulsatile and 5.0 ± 0.5 Llmin during nonpulsatile perfusion. Mean perfusion pressure was 86 ± 6.2 *Cardioplegic solution: 500 mllactated Ringer's, 10 mEq KCI, 12.5 mEq sodium bicarbonate, 12 ml 2% lidocaine, 17 ml 50% dextrose, 124 mg Solu-Cortef, pH 7.7, temperature 4° C. tRadioimmunoassay, New England Nuclear Biomedical Assay Laboratory, Boston, Mass. :j:Standarddeviation of the mean.
and 88 ± 5.6 mm Hg, respectively. Intraoperative urinary output averaged 5.0 ± 1.5 mIl min in the pulsatile perfusion and 5.3 ± 2 ml/min in the nonpulsatile perfusion groups. Postoperatively, it was difficult to accurately assess and compare urine output, as some patients had received diuretics and their fluid balances differed. All patients with postoperative hypertension, as defined in the Materials and patients section, became hypertensive from 0 to 6 hours postoperatively and were treated accordingly. Hypertension was present in 22 of 37 patients (60%) receiving pulsatile perfusion. In the subsequent 6 to 24 hours, 12 of these 22 patients (55%) required continued antihypertensive treatment. Among the patients subjected to nonpulsatile perfusion, 15 of 22 (68%) were hypertensive at 0 to 6 hours; from 6 to 24 hours, seven of these 15 patients (47%) still required nitroprusside. There was no significant difference (p > 0.05)* in the number of hypertensive patients between the two groups. Pre-CPB renin determinations averaged 2.8 ± 1.3 ng/mIlhr in the patients having pulsatile perfusion and 2.3 ± 0.4 ng/mIlhr in those having nonpulsatile perfusion (p > 0.05); after 30 minutes of normothermic perfusion, mean renin levels remained at 2.7 ± 1.2 and 2.7 ± 1.9 ng/mIlhr, respectively (p > 0.05). The hypertensive patients subjected to pulsatile perfusion had renin levels of 3.7 ± 1.9 ng/mIlhr, compared with 3.2 ± 0.7 ng/mIlhr for those having nonpulsatile perfusion (p > 0.05). The normotensive patients had renin levels of 2.6 ± 0.8 and 2.4 ± 0.5 ng/mIlhr, respectively. The difference in renin levels between hypertensive and normotensive patients was significant (p < 0.05), whereas the difference in renin between *Analysis of variance.
The Journal of
398
Salerno et al.
hypertensive patients in the pulsatile and nonpulsatile perfusion groups was not (p > 0.05). Intraoperative SPR was calculated at 1,600 ± 130 dynes/sec/em:" for the pulsatile and 1,760 ± 80 dynes/sec/em." for the nonpulsatile perfusion group (p > 0.05). Postoperative SPR was not calculated, because cardiac output is not routinely determined in our practice. Discussion Postoperative hypertension occurs in 33% to 58% of patients undergoing cardiac operations, 2-4 and the cause remains unknown. Nonpulsatile perfusion during CPB has been implicated as an etiologic factor, 4-6 and pulsatile flow appears to decrease the incidence of postoperative hypertension. S The systemic peripheral resistance (SPR) has been shown to be elevated during pulseless perfusion.v 4 whereas with pulsatile flow the SPR is significantly lower. 7. 8 The renin-angiotensin system and catecholamines'': 9 are contributing factors in this condition. A rise in peripheral renin levels has been demonstrated with nonpulsatile perfusion, possibly the result of either (1) direct stimulation of the juxtaglomerular apparatus by the absence of the pulse pressure" or (2) the redistribution of cortical blood flow due to vasoconstriction of the outer renal cortex. 10 Loss of pulse pressure during nonpulsatile CPB may also stimulate the carotid baroreceptors, so that the kidneys secrete more renin. 11 Pulsatile perfusion is also known to prevent the depressive effects on the pituitary gland observed during nonpulsatile flow. 12 In addition to the possible benefit of preventing postoperative hypertension, pulsatile perfusion appears to be more physiological than nonpulsatile flow. 6. 13. 14 Even so, surgeons have been reluctant to use it because of the unreliability of the systems available, the complexity of the apparatus, and the pressure gradients across the arterial cannula. Our study employed the technique of pulsatile perfusion described by Desjardin and associates. 1 This system delivers pulsatile perfusion which has a pressure tracing similar to normal cardiac action (Fig. 1). We 1S have demonstrated that the degree of hemolysis is comparable to that of nonpulsatile perfusion. Our results show that adding pulsatile perfusion to our standard American Optical roller pump did not affect the incidence of postoperative hypertension, as it occurred in 60% of the patients subjected to pulsatile perfusion and 68% of those subjected to nonpulsatile perfusion. In addition, renin levels were similar in the two groups during CPB and 2 hours after operation. It is interesting to note that both groups of patients had high renin levels even prior to CPB. The
Thoracic and Cardiovascular Surgery
reason for this observation, also noted by Frater, 16 remains unknown. It may be that factors such as diet, innate anxiety, and presurgical anxiety affect renin release in these patients. The hypertensive patients had higher renin levels postoperatively than the normotensive patients. However, there was a high variability in renin levels, as shown on the standard deviations of the mean. Thus nonpulsatile flow may not be the only underlying etiologic factor responsible for the hypertensive episode. For example, the mechanism may be a generalized disturbance related to the sympathetic overdrive, rather than resulting from improved cardiac performance after operation. 17 It has also been postulated that abnormal vasomotor responses may be involved, via an unstable feedback mechanism of the cardiac and/or aortic pressor receptors. 18-22 The role of catecholamines and other vasoactive agents, such as serotonin;" has been demonstrated previously in this condition. Since completion of this study we have routinely used pulsatile perfusion during CPB because of its theoretical advantages. However, we have been unable to decrease the incidence of hypertension after cardiac procedures. Much research remains to be done in this continuing effort to elucidate the mechanism underlying postoperative hypertension. REFERENCES Desjardin J, Maille JG, LussierCP, Grondin P: A simple device for achieving pulsatile flow during cardiopulmonary bypass. Ann Thorac Surg 27:178-180, 1979 2 Estefanous FG, Tarazi RC, Viljoen JF, EI Tawil MY: Systemic hypertension following myocardial revascularization. Am Heart J 85:732-738, 1973 3 Hoar PF, Hickey RF, Ullyot OJ: Systemic hypertension following myocardial revascularization. A method of treatment using epidural anesthesia. J THORAC CARDIOVASC SURG 71:859-864, 1976 4 Roberts AJ, Niarchos AP, Subramanian VA, Abel RM, Herman SO, Sealey JE, Case DB, White RP, Johnson GA, Laragh JH, Gay WA: Systemic hypertension associated with coronary artery bypass surgery. Predisposing factors, hemodynamic characteristics, humoral profile, and treatment. J THORAC CARDIOVASC SURG 74:846-859, 1977 5 Landyrnore RW, Murphy DA, Kinley CE, Parrott JG, Moffitt EA, Longley WJ, Qirbi AA: Does pulsatile flow influence the incidence of postoperative hypertension? Ann Thorac Surg 28:261-268, 1979 6 Many M, Giron G, Birtwell WC, Deterling RA Jr, Soroff HS: Effectsof depulsation of renal blood flow upon renal function and renin secretion. Surgery 66:242-249, 1969 7 Jacobs LA, Klopp EH, Seamone W, Topaz SR, Gott VL: Improved organ function during cardiac bypass with a
Volume 81
Hypertension after coronary operation
Number 3
3 99
March,1981
roller pump modified to deliver pulsatile flow. J THORAC CARDIOVASC SURG 58:703-712, 1969 8 Trinkle JK, Helton NE, Bryant LR, Griffen WO: Pulsatile cardiopulmonary bypass. Clinical evaluation. Surgery
16 17
68:1074-1078, 1970 9 Laragh JH, Baer L, Brunner HR, Buhler FR, Sealey JE, Vaughan DE: Renin, angiotensin and aldosterone system in pathogenesis and management of hypertensive vascular disease. Am J Mcd 52:633-652, 1972 10 Goodman TA, Gerard DF, Bernstein EF, Dilley RB: The effects of pulseless perfusion on the distribution of renal cortical blood flow and on renin release. Surgery 80:31-
39, 1976 II Edmunds LH: Discussion of Landymore et aP 12 Taylor KM, Wright GS, Bain WH, Caves PK, Beastall GS: Comparative studies of pulsatile and nonpulsatile flow during cardiopulmonary bypass. III. Response of anterior pituitary gland to thyrotropin-releasing hormone. J THORAC CARDIOVASC SURG 75:579-584, 1978 13 Dunn J, Kirsh MM, Harness J, Carroll M, Straker J, Sloan H: Hemodynamic, metabolic, and hemotologic effects of pulsatile cardiopulmonary bypass. J THORAC CARDIOVASC SURG 68:138-147, 1974 14 Salerno TA, Shizgal HM, Dobell ARC: Pulsatile perfusion. Its effects on blood flow distribution in hypertrophied hearts. Ann Thorac Surg 27:559-563, 1979 15 Salerno TA, Charrette EJP, Keith FM: Hemolysis during
18
19 20
pulsatile perfusion. Clinical evaluation of a new device. J THORAC CARDIOVASC SURG 79:579-581, 1980 Frater RWM: Discussion of Landymore et al 5 Fouad FM, Estefanous FG, Tarazi RC: Hemodynamics of postmyocardial revascularization hypertension. Am J Cardiol 41:564-569, 1978 Estefanous FG, Tarazi RC, Buckley S, Taylor PC: Arterial hypertension in immediate postoperative period after valve replacement. Br Heart J 40:718-724, 1978 Viljoen JF, Estefanous FG, Tarazi RC: Acute hypertension immediately after coronary artery surgery. J THORAC CARDIOVASC SURG 71:548-550, 1976 Hanson EL, Kane PB, Askanazi J, Neville JF, Webb WR: Comparison of patients with coronary artery or valve disease. Intraoperative differences in blood volume and observations of vasomotor response. Ann Thorac Surg
22:343-346, 1976 21 Liard JF, Tarazi RC, Ferrario CM, Manger WM: Hemodynamic and humoral characteristics of hypertension induced by prolonged stellate ganglion stimulation in conscious dogs. Circ Res 36:455-464, 1975 22 Peterson DF, Brown AM: Pressor reflexes produced by stimulation of afferent fibers in cardiac sympathetic nerves of the cat. Circ Res 28:605-610, 1971 23 Replogle R, Levy M, DeWall RA, Lillehei RC: Catecholamine and serotonin response to cardiopulmonary bypass. J THORAC CARDIOVASC SURG 44:638-648, 1962